Mitochondria—Energy and Health

Mitochondria are the powerhouses of the cell.

Figure 1. A single mitochondrion on the right, and the mitochondria in the cell on the left.

Mitochondria are membrane-bound cell organelles that generate chemical energy needed to power processes in the cell. Chemical energy produced by the mitochondria is stored in a small molecule called adenosine triphosphate (ATP).

Figure 2. Molecular structure of ATP.

The average cell uses 10 billion ATP per day!

ATP cannot be stored for later, therefore the mitochondria must function consistently all the time (primarily within muscles, brain, liver, heart and gastrointestinal tract). There are about 250 g of ATP in the cells at all time, this represents about 4.25 watts, (~AA battery). Every day, a healthy person produces a remarkable 1200 watts!

Figure 3. Amount of energy in the cells equals one AA battery

What if there is not enough ATP?

ATP is used as the primary energy source for most biochemical and physiological processes, such as growth, movement and homeostasis. Brain uses 70% of ATP that was produced. If ATP production is not adequate, because mitochondria are not functioning properly, neurodegeneration can occur. There is a strong correlation between mitochondrial dysfunction and neurodegeneration in disease such as:

  •       Amyotrophic lateral sclerosis (ALS)
  •       Alzheimer’s disease
  •       Autism
  •       Dementia
  •       Huntington’s disease
  •       Parkinson’s disease

 Mitochondrial dysfunction can also cause or aggravate other conditions such as:

  •       Cardiovascular disease
  •       Chronic fatigue syndrome
  •       Diabetes
  •       Migraine headache

What do mitochondria need to function properly?

There are three essential process for ATP production which include:

  1.     β-Oxidation of fats,
  2.     Citric acid cycle and
  3.     Oxidative phosphorylation (OXPHOS).

ß-oxidation is the catabolic process by which fatty acid molecules are broken down in the mitochondria to generate acetyl-CoA (which enters the citric acid cycle) and NADH and FADH2 (which are co-enzymes used in the electron transport chain which is part of OXPHOS).

Essential Nutrients for this step are:

  •         FAD (riboflavin), NADH (niacin), CoQ10
  •         Carnitine to transport fatty acids

Citric acid cycle, also known as the Krebs cycle or the TCA cycle (tricarboxylic acid cycle) is a series of chemical reactions which release stored energy through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins.

Essential Nutrients for this step are:

  •     Iron, magnesium, manganese
  •     B1, B2, B3
  •     Cysteine (glutathione), lipoate

Oxidative phosphorylation. (OXPHOS) produces ATP by using molecules produced in the citric acid cycle and oxygen molecule in the processes on the electron transport chain and by chemiosmosis. The electron transport chain consists of a series of proteins and molecules located in the inner membrane of the mitochondria. Electrons are passed from one complex to another in a series of redox reactions. This creates a proton gradient, which is needed to make ATP by the enzyme called ATP synthase in a process called chemiosmosis.

Figure 4.Scheme of OXPHOS

Essential Nutrients for these steps are:

  •     CoQ10 (transports high-energy electrons)
  •     Riboflavin (complex II)
  •     NADH (niacin)
  •     Magnesium

Where does damage come from?

  •     Oxidants leaked while ATP is produced
  •     Aging (accumulated oxidative damage to DNA of mitochondria)
  •     Genomic susceptibility
  •     Toxic metals
  •     Persistent organic pollutants
  •     Some medications
  •  Alcohol

How can I make my mitochondria powerful and healthy?,

  1.     Optimize nutrient status that facilitate mitochondrial ATP production
  •         Get enough essential nutrients (though food and supplementation) for each step of ATP production: FAD (riboflavin), NADH (niacin), CoQ10, carnitine iron, magnesium, manganese, B1;B2,B3, Cysteine (glutathione), lipoate
  1.     Decrease toxin exposure
  2.     Provide nutrients that protect the mitochondria from oxidative stress.

Eating a diet rich in fruit, vegetables and omega-3 fats as well as taking supplements for antioxidant protection.

  1.     Build muscle mass

Hot topics –mitochondria- 2022/2023 (key words)

  •         ,,Neurodegenerative diseases, including Parkinson’s disease, are linked to the accumulation of defective mitochondria in the brain and to microbial dysbiosis in the gut. However, the interplay between these factors is incompletely understood. Fedele et al. reveal how gut mitochondrial dysfunction activates intestinal inflammation to drive neurodegeneration in a Parkinson’s disease model.´´ Aparicio, R., Schmid, E.T. & Walker, D.W. Gut mitochondrial defects drive neurodegeneration. Nat Aging 2, 277–279 (2022).
  •         Compromised clearance of dysfunctional mitochondria, through the process of mitophagy, has garnered attention as an essential contributor to aging and neurodegeneration. Schmid and colleagues reveal that genetic enhancement of mitophagy via neuronal overexpression of BNIP3 alleviates brain aging and prolongs healthspan in fruit flies. Lautrup, S., Fang, E.F. Enhanced brain mitophagy slows systemic aging. Nat Aging 2, 463–464 (2022).

·         Mitochondrial dysfunction is central in biological aging, but experimentally controlling mitochondria in vivo to test causality has been difficult. Optogenetically preserving mitochondrial function with age addressed this difficulty and increased lifespan and healthspan in Caenorhabditis elegans. Harnessing light energy to charge mitochondria and extend lifespan. Nat Aging 3, 151–152 (2023).


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Houten, S. M., & Wanders, R. J. (2010). A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation. Journal of inherited metabolic disease, 33(5), 469–477.

Lowenstein, J. M. (1969). Methods in Enzymology, Volume 13: Citric Acid Cycle. Boston: Academic Press. ISBN 978-0-12-181870-8.


Kay J, Weitzman PD (1987). Krebs’ citric acid cycle: half a century and still turning. London: Biochemical Society. pp. 25. ISBN 978-0-904498-22-6. (updated: February 16, 2023)